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dc.contributor.authorDaliri, Ayouben_US
dc.contributor.authorElizabeth, Heller Murrayen_US
dc.contributor.authorBlood, Anneen_US
dc.contributor.authorBurns, Jamesen_US
dc.contributor.authorNoordzij, J. Pieteren_US
dc.contributor.authorNieto-Castanon, Alfonsoen_US
dc.contributor.authorTourville, Jasonen_US
dc.contributor.authorGuenther, Franken_US
dc.date.accessioned2020-04-15T14:45:42Z
dc.date.available2020-04-15T14:45:42Z
dc.date.issued2020-02
dc.identifier.citationAyoub Daliri, Heller Murray Elizabeth, Anne Blood, James Burns, J. Pieter Noordzij, Alfonso Nieto-Castanon, Jason Tourville, Frank Guenther. 2020. "Auditory feedback control mechanisms do not contribute to cortical hyperactivity within the voice production network in adductor spasmodic dysphonia." Journal of Speech, Language, and Hearing Research, Volume 63, Issue 2, pp. 421 - 432. https://doi.org/10.1044/2019_JSLHR-19-00325
dc.identifier.urihttps://hdl.handle.net/2144/40173
dc.description.abstractAdductor spasmodic dysphonia (ADSD), the most common form of spasmodic dysphonia, is a debilitating voice disorder characterized by hyperactivity and muscle spasms in the vocal folds during speech. Prior neuroimaging studies have noted excessive brain activity during speech in ADSD participants compared to controls. Speech involves an auditory feedback control mechanism that generates motor commands aimed at eliminating disparities between desired and actual auditory signals. Thus, excessive neural activity in ADSD during speech may reflect, at least in part, increased engagement of the auditory feedback control mechanism as it attempts to correct vocal production errors detected through audition. To test this possibility, functional magnetic resonance imaging was used to identify differences between ADSD participants and age-matched controls in (i) brain activity when producing speech under different auditory feedback conditions, and (ii) resting state functional connectivity within the cortical network responsible for vocalization. The ADSD group had significantly higher activity than the control group during speech (compared to a silent baseline task) in three left-hemisphere cortical regions: ventral Rolandic (sensorimotor) cortex, anterior planum temporale, and posterior superior temporal gyrus/planum temporale. This was true for speech while auditory feedback was masked with noise as well as for speech with normal auditory feedback, indicating that the excess activity was not the result of auditory feedback control mechanisms attempting to correct for perceived voicing errors in ADSD. Furthermore, the ADSD group had significantly higher resting state functional connectivity between sensorimotor and auditory cortical regions within the left hemisphere as well as between the left and right hemispheres, consistent with the view that excessive motor activity frequently co-occurs with increased auditory cortical activity in individuals with ADSD.en_US
dc.format.extentpp. 421 - 432.en_US
dc.language.isoen_US
dc.publisherAmerican Speech-Language-Hearing Associationen_US
dc.relation.ispartofJournal of Speech, Language, and Hearing Research
dc.subjectClinical sciencesen_US
dc.subjectCognitive sciencesen_US
dc.subjectLinguisticsen_US
dc.subjectSpeech-language pathology & audiologyen_US
dc.subjectFeedforwarden_US
dc.subjectSpasmodic dysphoniaen_US
dc.subjectAuditory feedbacken_US
dc.subjectVoiceen_US
dc.titleAuditory feedback control mechanisms do not contribute to cortical hyperactivity within the voice production network in adductor spasmodic dysphoniaen_US
dc.typeArticleen_US
dc.description.versionFirst author draften_US
dc.identifier.doi10.1044/2019_JSLHR-19-00325
pubs.elements-sourcemanual-entryen_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Health & Rehabilitation Sciences: Sargent Collegeen_US
pubs.organisational-groupBoston University, College of Health & Rehabilitation Sciences: Sargent College, Speech, Language & Hearing Sciencesen_US
pubs.publication-statusPublisheden_US
dc.identifier.mycv454458


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